Our long-range goal is to achieve an understanding of the mechanisms of reproductive cyclicity, by achieving an understanding of the dynamic interrelationships between the gonads and the anterior pituitary. (1) We are studying the ovarian negative feedback signals, the removal of which lead to a prompt increase in serum FSH. Included among these signals may be the "follicular fluid meiosis inhibitor". (2) We are seeking to understand what prevents serum LH from rising before four days after ovariectomy, using adrenalectomy and MER-25 (an estrogen inhibitor) as tools. (3) We are investigating why the prompt FSH and LH response in male rats which follows orchidectomy, is abolished by adrenalectomy, and also to investigate a good animal model to test "inhibin". (4) We will follow the steroid and gonadotrophin response to porta-caval shunt, which reduces steroid MCR. (5) We would like to correlate morphology and hormone content in atrophied pituitaries following MER treatment. (6) What is the mechanism by which the proestrous LH surge is blocked by pentobarbital given 24 hours before at diestrus? (7) What is the mechanism by which LH injection induces endogenous FSH secretion in pentobarbital-blocked proestrous rats? (8) Does the secondary, prolonged FSH rise between proestrus and estrus recruit the next follicle pool for ovulation? (9) What is the mechanism by which follicles are doubled in compensatory ovulation, following unilateral orchidectomy? (10) What pituitary hormones will serve as adequate replacement therapy to complete the ovarian cycle in rats hypophysectomized on the morning of the day before proestrus?